Gaining or losing a chromosome, a condition known as aneuploidy, is often caused by stress, and is known to have detrimental consequences, including a variety of human diseases. But according to new research in yeast published online today (January 30) in Nature, stress-induced aneuploidy may also help organisms adapt, conferring an adaptive advantage to yeast cells in the face of continued stress.

“It’s in interesting study,” said Judith Berman, a molecular geneticist at the University of Minnesota who was not involved in the research. Berman’s own work in Candida albicans yeast supports the idea that aneuploidy has adaptive functions, she said, and the new study highlights aneuploidy’s underappreciated role in generating genetic and phenotypic diversity.

Aneuploidy, and the question of cause or effect, plagues cancer biologists, said Elton T. Young, a biochemist at the University of Washington who also did not participate in the research. Cancer cells are known to have many chromosomal irregularities, often including extra chromosomes, for example, but it’s always been unclear whether aneuploidy causes tumorigenesis, or is merely a symptom of the cancerous state. “I think this opens up a new way to approach that old question,” Young said.

Earlier work by Rong Li at Stowers Institute for Medical Research in Missouri and her colleagues showed that cells whose ability to divide was crippled by the loss of a motor protein found quick and “creative” ways to keep growing, Li explained. These cells had made stable, heritable genetic changes that were not small point mutations—they had acquired extra chromosomes.

“We called this adaptation the ‘big bang’ because it was so abrupt,” said Li. It raised a new question—what if it wasn’t the loss of a specific protein that was causing aneuploidy, but simply the stress the cells were under?

In the current study, Li’s group surveyed the effects of a variety of stressors, including excess oxygen and drugs that block key cellular processes, on Saccharomyces cerevisiae yeast. “We were looking for a big general stressor,” she explained. “We didn’t want to focus on a specific pathway.”

Indeed, most of the stressors studied increased the rate of aneuploidy by about 10-fold. But one of these stressors, a drug called radicicol, which targets the heat shock protein Hsp90, caused 100-fold higher levels of aneuploidy. And sure enough, all of the colonies that managed to survive the drug carried an extra copy of chromosome XV, suggesting that aneuploidy was conferring a growth advantage in the presence of radicicol.

The researchers tracked this advantage to a few gene candidates on chromosome XV that likely conferred radicicol resistance. When those genes were deleted, the yeast faltered, losing their ability to grow robustly in the drug’s presence. Taken together, the results suggested that aneuploidy confers resistance by increasing the copy number of several relevant genes.

Radicicol-induced anueploidy also appeared to help yeast adapt to new stressors. Compared to untreated S. cerevisae, radicicol-treated yeast grew better when exposed to drugs such as fluconazole, an anti-fungal, or tunicamycin, a glycosylation inhibitor, and most of the drug-resistant colonies were aneuploid.

Aneuploidy had a “dramatic impact,” Li said, which might explain why yeast often thrive when confronted with sudden toxic conditions. Point mutations may confer little or no change, but adding or deleting a whole chromosome and all the genes it carries always changes phenotype, Li noted.

“It’s always exciting to see investigations into stress-induced mutagenesis,” said Susan Rosenberg, who researches the molecular basis of genome instability and evolution at the Baylor College of Medicine. And if a similar phenomenon is identified in other eukaryotic cells, such as mammalian cells, it may have implications for cancer, Li added. Given that aneuploidy is a hallmark of tumor cells, it may be conferring selective advantages that allow them to quickly escape the toxic sledgehammer of chemotherapy drugs, she said.

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This means, stress in general gives adoptability via aneuploidy,does this implies stressed human have traits, which will take himÂ far(lost cells under stress are not counted,gladiators) against unstressed man.

It's frustrating to see so many assertions concerning "adaptation" based on standard models used in research.Â To report on something that occurs with a single celled model organism, that multiplies by dividing, is fine as far as it goes.Â It would be interesting to be provided with an example in, say, a human or an elephant, where a signal cascade follow even one stimulus must in some instances go scores ofÂ transductions before producing an appropriate response, and where the entire complex cascade must not only be absolutely complete to work as it does but, also, each step along the way must be in its precise proper place in the sequence.Â Add to this what could be aptly called "the somatic/germline barrier," whereby the DNA involved in reproduction is a whole 'nuther ball game, than the homeostatic system that is separate from it.

Recently, in another article, the fact that yeast organisms sometimes cluster together into clumps illustrates how single-celled organisms became complex, sexually-reproducing species.

I'm not saying it didn't happen.Â I cannot help seeing such assertions as analogous to comparing what might occur in a box of Lincoln Logs to how a skyscraper is constructed.

What a phenomenon is, is what it is.Â But if it is one piece of a puzzle of a billion pieces, then it hardly illustrates how the puzzle functions.

This synopsis seems to indicate some causal link between the stress and aneuploidy. However, theÂ synopsis provided above seems to report a garden-variety,Â selective pressure to weed out all yeast except thoseÂ that happen to already have aÂ specific extra chromsome that has some genes conferring drug resistance. This is not causal but consequence. Moreover, such selections are not new, unusual or unexpected. It's called evolution.

Perhaps the report in Nature, which I have not yet read, is clearer than this synposis about why the observations are considered interesting?? This would be novel if some pathway had been found that, for example, senses stress and alters some component of mitosis that leads to a higherÂ likelihood that a daughter cell isÂ aneuploid.Â It is a tricky type of experiment to establish whether each cell division is more, less or equally likely to have an aneuploid outcome under selective and non-selective conditions. If more likely to be aneuplod, then deleting the identified genes would reduce the aneuploidy rate to baseline. That collectively wouldÂ suggest that those genes are part of some adaptive mechanism in which an active stress responseÂ can lead to aneuploidy. Maybe that is what has been done. But the report in the Scientist doesn'tÂ suggest that. Instead, as written, the report suggests nothing new.Â

This means, stress in general gives adoptability via aneuploidy,does this implies stressed human have traits, which will take himÂ far(lost cells under stress are not counted,gladiators) against unstressed man.

It's frustrating to see so many assertions concerning "adaptation" based on standard models used in research.Â To report on something that occurs with a single celled model organism, that multiplies by dividing, is fine as far as it goes.Â It would be interesting to be provided with an example in, say, a human or an elephant, where a signal cascade follow even one stimulus must in some instances go scores ofÂ transductions before producing an appropriate response, and where the entire complex cascade must not only be absolutely complete to work as it does but, also, each step along the way must be in its precise proper place in the sequence.Â Add to this what could be aptly called "the somatic/germline barrier," whereby the DNA involved in reproduction is a whole 'nuther ball game, than the homeostatic system that is separate from it.

Recently, in another article, the fact that yeast organisms sometimes cluster together into clumps illustrates how single-celled organisms became complex, sexually-reproducing species.

I'm not saying it didn't happen.Â I cannot help seeing such assertions as analogous to comparing what might occur in a box of Lincoln Logs to how a skyscraper is constructed.

What a phenomenon is, is what it is.Â But if it is one piece of a puzzle of a billion pieces, then it hardly illustrates how the puzzle functions.

This synopsis seems to indicate some causal link between the stress and aneuploidy. However, theÂ synopsis provided above seems to report a garden-variety,Â selective pressure to weed out all yeast except thoseÂ that happen to already have aÂ specific extra chromsome that has some genes conferring drug resistance. This is not causal but consequence. Moreover, such selections are not new, unusual or unexpected. It's called evolution.

Perhaps the report in Nature, which I have not yet read, is clearer than this synposis about why the observations are considered interesting?? This would be novel if some pathway had been found that, for example, senses stress and alters some component of mitosis that leads to a higherÂ likelihood that a daughter cell isÂ aneuploid.Â It is a tricky type of experiment to establish whether each cell division is more, less or equally likely to have an aneuploid outcome under selective and non-selective conditions. If more likely to be aneuplod, then deleting the identified genes would reduce the aneuploidy rate to baseline. That collectively wouldÂ suggest that those genes are part of some adaptive mechanism in which an active stress responseÂ can lead to aneuploidy. Maybe that is what has been done. But the report in the Scientist doesn'tÂ suggest that. Instead, as written, the report suggests nothing new.Â

This means, stress in general gives adoptability via aneuploidy,does this implies stressed human have traits, which will take himÂ far(lost cells under stress are not counted,gladiators) against unstressed man.

It's frustrating to see so many assertions concerning "adaptation" based on standard models used in research.Â To report on something that occurs with a single celled model organism, that multiplies by dividing, is fine as far as it goes.Â It would be interesting to be provided with an example in, say, a human or an elephant, where a signal cascade follow even one stimulus must in some instances go scores ofÂ transductions before producing an appropriate response, and where the entire complex cascade must not only be absolutely complete to work as it does but, also, each step along the way must be in its precise proper place in the sequence.Â Add to this what could be aptly called "the somatic/germline barrier," whereby the DNA involved in reproduction is a whole 'nuther ball game, than the homeostatic system that is separate from it.

Recently, in another article, the fact that yeast organisms sometimes cluster together into clumps illustrates how single-celled organisms became complex, sexually-reproducing species.

I'm not saying it didn't happen.Â I cannot help seeing such assertions as analogous to comparing what might occur in a box of Lincoln Logs to how a skyscraper is constructed.

What a phenomenon is, is what it is.Â But if it is one piece of a puzzle of a billion pieces, then it hardly illustrates how the puzzle functions.

This synopsis seems to indicate some causal link between the stress and aneuploidy. However, theÂ synopsis provided above seems to report a garden-variety,Â selective pressure to weed out all yeast except thoseÂ that happen to already have aÂ specific extra chromsome that has some genes conferring drug resistance. This is not causal but consequence. Moreover, such selections are not new, unusual or unexpected. It's called evolution.

Perhaps the report in Nature, which I have not yet read, is clearer than this synposis about why the observations are considered interesting?? This would be novel if some pathway had been found that, for example, senses stress and alters some component of mitosis that leads to a higherÂ likelihood that a daughter cell isÂ aneuploid.Â It is a tricky type of experiment to establish whether each cell division is more, less or equally likely to have an aneuploid outcome under selective and non-selective conditions. If more likely to be aneuplod, then deleting the identified genes would reduce the aneuploidy rate to baseline. That collectively wouldÂ suggest that those genes are part of some adaptive mechanism in which an active stress responseÂ can lead to aneuploidy. Maybe that is what has been done. But the report in the Scientist doesn'tÂ suggest that. Instead, as written, the report suggests nothing new.Â

In the literature there is a lot of confusion related to the real meaning of adaptation in biology. if an organism is adapted to a certain condition, it does not mean that this organism changed its genes (mutated) to adapt to the new condition. Rather, there has been selection of individuals within the population that have the necessary genes (mutated genes) to adapt to the new condition.

In the case of the study above, as FFScientistÂ mention, there is a big probability that among yeast population tested some had already a specific extra chromosome that confer drug resistance. that is to say stress is not theÂ cause of aneuploidy, but rather stress selected forÂ those yeast cells that happens to be aneuploids.Â

In the literature there is a lot of confusion related to the real meaning of adaptation in biology. if an organism is adapted to a certain condition, it does not mean that this organism changed its genes (mutated) to adapt to the new condition. Rather, there has been selection of individuals within the population that have the necessary genes (mutated genes) to adapt to the new condition.

In the case of the study above, as FFScientistÂ mention, there is a big probability that among yeast population tested some had already a specific extra chromosome that confer drug resistance. that is to say stress is not theÂ cause of aneuploidy, but rather stress selected forÂ those yeast cells that happens to be aneuploids.Â

In the literature there is a lot of confusion related to the real meaning of adaptation in biology. if an organism is adapted to a certain condition, it does not mean that this organism changed its genes (mutated) to adapt to the new condition. Rather, there has been selection of individuals within the population that have the necessary genes (mutated genes) to adapt to the new condition.

In the case of the study above, as FFScientistÂ mention, there is a big probability that among yeast population tested some had already a specific extra chromosome that confer drug resistance. that is to say stress is not theÂ cause of aneuploidy, but rather stress selected forÂ those yeast cells that happens to be aneuploids.Â

As the author of this paper, it is my pleasure to addressing the questions posted here.Â

For FJScientist and Tanos' question on whether the appearance of aneuploidy is a result of pure selection or actually involved induction: To measure the chromosome loss rate, we use a selectively neutral artificial chromosome, whose gain and loss can be easily monitored, and do not impose significant fitness change.Â

For keepitlegal's comment on how general this mechanism of adaptation exist beyond the lab environment: Due to the lack of proper testing system as stated above, the exact chromosome loss rate cannot be determined in many other species. However, it is becoming more and more clear that aneuploidy (whole chromosome copy number variation) is a widespreading mutation, but not a monster created only in the lab. It has been isolated from all kinds of industrial yeast as well as some yeasts from natural habitat. In fact, as I recently found, the Redstar baking yeast sold in Costco has a highly imbalanced genome. On the other hand, aneuploidy is a hallmark of cancer, a result of somatic evolution process.Â

As the author of this paper, it is my pleasure to addressing the questions posted here.Â

For FJScientist and Tanos' question on whether the appearance of aneuploidy is a result of pure selection or actually involved induction: To measure the chromosome loss rate, we use a selectively neutral artificial chromosome, whose gain and loss can be easily monitored, and do not impose significant fitness change.Â

For keepitlegal's comment on how general this mechanism of adaptation exist beyond the lab environment: Due to the lack of proper testing system as stated above, the exact chromosome loss rate cannot be determined in many other species. However, it is becoming more and more clear that aneuploidy (whole chromosome copy number variation) is a widespreading mutation, but not a monster created only in the lab. It has been isolated from all kinds of industrial yeast as well as some yeasts from natural habitat. In fact, as I recently found, the Redstar baking yeast sold in Costco has a highly imbalanced genome. On the other hand, aneuploidy is a hallmark of cancer, a result of somatic evolution process.Â

As the author of this paper, it is my pleasure to addressing the questions posted here.Â

For FJScientist and Tanos' question on whether the appearance of aneuploidy is a result of pure selection or actually involved induction: To measure the chromosome loss rate, we use a selectively neutral artificial chromosome, whose gain and loss can be easily monitored, and do not impose significant fitness change.Â

For keepitlegal's comment on how general this mechanism of adaptation exist beyond the lab environment: Due to the lack of proper testing system as stated above, the exact chromosome loss rate cannot be determined in many other species. However, it is becoming more and more clear that aneuploidy (whole chromosome copy number variation) is a widespreading mutation, but not a monster created only in the lab. It has been isolated from all kinds of industrial yeast as well as some yeasts from natural habitat. In fact, as I recently found, the Redstar baking yeast sold in Costco has a highly imbalanced genome. On the other hand, aneuploidy is a hallmark of cancer, a result of somatic evolution process.Â